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. Author manuscript; available in PMC: 2015 Apr 16.
Published in final edited form as: Oncogene. 2013 Oct 21;33(42):4997–5005. doi: 10.1038/onc.2013.437

Figure 5.

Figure 5

Accelerated HCC and CC formation and GRP78 re-expression in cPf/f78f/f livers. (a) Kaplan-Meier plot of WT, cPf/f, cPf/f78f/+ and cPf/f78f/f mice showing tumor nodule-free percentage over time. n=3 to 11 for each genotype at each time point. (b) Upper: H&E staining of liver sections from WT and cPf/f78f/f mice at 8–9 months. cPf/f78f/f mice showed histological features of HCC and CC. Lower: immunohistochemistry staining of GRP78 on liver sections of WT mice and tumor sections from cPf/f78f/f mice aged 8–9 months. (c) H&E staining of liver tumor sections from cPf/f and cPf/f78f/+ mice at 12 months, which showed the presence of both HCC and CC. Scale bars show 100 µm and are applicable to panels b and c. (d) Schematic model of tumor development in cPf/f78f/f mice. Hepatic GRP78 expression level at each stage corresponds to the color gradient bar on the upper left corner. The major phenotypes at each stage are indicated below. BD: bile duct; PV: portal vein.